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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth inhibition or stimulation of target adenocarcinoma cells in rats sensitized with spleen cells from syngeneic tumor-bearing rats was significantly suppressed in colony inhibition assays when the spleen cells were treated in vitro with 0.8 mug progesterone or more/ml medium. In addition, when tumor-bearing rats were treated with 1 mg medroxyprogesterone acetate weekly in vivo, the inhibiting action of the spleen cells from rats with regressed tumors was also suppressed. Progesterone thus suppressed immune spleen cells in vivo and in vitro.
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PMID:In vivo and in vitro tests of inhibitory effect of progesterone on cell-mediated immunity in rats bearing a syngeneic uterine adenocarcinoma. 109 43

Progesterone, like estrogens, is used in the treatment of metastatic breast cancer. The 3 most active derivatives are megestrol, norethisterone acetate, and medroxyprogesterone acetate (MPA). This study evaluates the use of MPA in treating metastatic breast cancer in 40 postmenopausal women (average age, 63 years; average duration of postmenopause, 14 years) who have either not responded to or have relapsed after therapy with estrogens and androgens. 18 patients received a depot preparation of MPA intramuscularly in a loading dose of 3.2 g over a 2-week period and then 400 mg at 2-4 week intervals. 22 patients received the drug orally in a dose of 200 to 300 mg daily. Patients were evaluated after 6 weeks of therapy. Criteria for evaluating response were those used by the Eastern Cooperative Oncology Group. Only 2 of 40 patients exhibited an objective response (disappearance of metastatic lymph node for 9 months in 1 and well-documented clinical improvement and control of brain metastases for 22 months in another). 2 patients had mixed responses of chest wall metastases (regression of some but not all lesions) lasting 3 and 4 months respectively. 5 patients had obvious subjective response (pain relief) but no objective response. Overall response rate was 22%: 4 objective responses (10%) and 5 subjectives responses (12%). Route of administration did not correlate with response. Tumor stimulation and clinical deterioration occurred in 4 patients. It appears that MPA therapy is costly and of minimal usefulness as secondary therapy in metastatic breast cancer. Further studies should focus on megestrol and norethisterone acetate which have been documented to have better response rates.
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PMID:Response to medroxyprogesterone acetate (NSC-26386) as secondary hormone therapy for metastatic breast cancer in postmenopausal women. 126 Jul 80

The effects of estrogen, progesterone, and testosterone on the growth of 7,12 dimethylbenz(a)anthracene (DMBA) induced adenocarcinomas in rats (Wistar strain) were evaluated. Estrogen resulted in the highest acceleration of tumor volume. The histologic features were a solid structure associated with a significant proliferation of connective tissues and with many signet ring cells with intracytoplasmic canaliculi. Progesterone changed the histologic features to a more immature adenocarcinoma associated with a notable solid area with many mitotic figures, although the growth rate of the tumor was the same as the controls. On the contrary, testosterone induced the slowest tumor growth and a histologically scirrhus pattern. The results of this preliminary observation indicate a possible role for sex steroids in the ovarian tumorigenic process.
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PMID:A study of the role of sex hormones in rat ovarian cancer. 130 11

The cytostatic effect of medroxyprogesterone acetate (MPA; an oral luteohormone preparation) on two cell lines of ovarian carcinoma cultured in vitro (SHIN-3 and MN-1) was studied. At the same time, changes in the morphology and colony formation of these cancer cells after exposure to the drug were examined. 1) The doubling time of SHIN-3 cells in the logarithmic growth phase was prolonged 2.5 times at a MPA dose of 10(-8)M and 3.2 times at a MPA dose of 10(-5)M. The drug, however, exerted no significant cytostatic effect on MN-1 cells. 2) When the IC50 of MPA was assessed by counting live SHIN-3 cells in an FCS-added medium, it was 2.7 x 10(-5)M. When the same assessment was done with a medium without serum, IC50 was 6.4 x 10(-6)M. 3) After 120 hours of incubation in a medium containing 10(-8)M of MPA, CA125 (a tumor marker) production by SHIN-3 cells was suppressed by 35%. The suppression rate was 79% for SHIN-3 cells incubated in a medium containing 10(-5) of MPA. 4) The cytoplasm of SHIN-3 cells, incubated in a MPA-added medium, showed the formation of small mucous vacuoles and expansive degeneration, accompanied by a marked increase in size and thinning of the nucleus. 5) In an experiment on colony formation with collagen gel, the colony size decreased MPA concentration dependently, and was accompanied by the appearance of lobulated colonies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antiproliferative actions of medroxyprogesterone acetate (MPA) to human ovarian cancer cell lines in vitro]. 131 10

A 55-year-old female with severe inflammatory breast cancer was treated with the combined use of MPA and the intraarterial infusion chemotherapy. One cycle consisted of 4'-epi-adriamycin; 210 mg (day 1, 4 and 8) and daily administration of MPA; 1,200 mg. A marked shrinkage of the tumor was obtained with this treatment. The regressive change was noted not only in the primary lesion but in lymph nodes of the axillary region. Therefore, the combined use of MPA with intra-arterial infusion chemotherapy may well contribute to the treatment of inflammatory breast cancer.
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PMID:[A case of inflammatory breast cancer treated with medroxyprogesterone acetate (MPA) in combination with intra-arterial infusion chemotherapy]. 138 77

Twenty-six patients with advanced renal cell carcinoma were treated with suramin administered by continuous infusion, with dosing determined by a nomogram. One patient achieved a partial response and five patients achieved a minor response or had stable disease for > 3 months. Toxicities included an immune-mediated thrombocytopenia in one patient and Staphylococcus sepsis that was not associated with neutropenia in five patients. Pharmacokinetic parameters were determined by the ADAPT II MAP-Bayesian parameter estimation program. Patient data were fit using a two-compartment open model and first-order rate elimination. This showed a wide interpatient variation in time to target level (median, 13.8 days), volume of distribution (median, 15.2 liters/m2), and t1/2-beta (median, 20.6 days). The patients who achieved a partial response, minor response, or stable disease had a slower elimination rate of suramin, compared to patients with progressive disease. Tumor specimens were obtained prior to therapy and were analyzed for the production of five different growth factor-specific RNA transcripts. These included transforming growth factor alpha, acidic fibroblast growth factor, basic fibroblast growth factor, and platelet-derived growth factor types A and B. No difference in the pattern of growth factor expression was seen in tumors of responding and nonresponding patients. Suramin does not have significant antitumor activity in renal cell carcinoma. The wide variability in pharmacokinetics suggests that individual dosing should be used in future trials of suramin for treatment for other malignancies. Pertinent corollary studies of tumor biology and clinical pharmacology should be included whenever possible in clinical trials in patients with renal cell carcinoma.
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PMID:Phase II trial of suramin in patients with advanced renal cell carcinoma: treatment results, pharmacokinetics, and tumor growth factor expression. 139 2

The highly (ASML) and non metastatic (AS) variants of the rat tumor BSp73 were compared with respect to cell surface carbohydrate proteins. Fluorescence labelling with lectins (ConA, MPA, PNA, SBA, UEA-I, WGA) revealed a differentiated carbohydrate pattern at the cell surface of these cell lines. The highly metastatic variant was significantly more glycosylated with respect to galactosyl, mannosyl and N-acetylgalactosylamine residues; fucosyl residues were exclusively expressed in the metastatic variant. Examination of isolated plasma membrane fractions showed quantitative differences with respect to glycosylated proteins separated on polyacrylamide gels. A 30 kDa glycoprotein (GP30-ASML) dominant in the metastatic variant was further characterized. Various detergents (CHAPS, Nonidet, SDS, Triton X-100) and urea extracted it exclusively from the highly metastatic variant. GP30-ASML is a predominantly O-glycosylated single polypeptide chain with terminal N-acetylgalactosamine and galactosyl residues; its molecular weight determined by SDS-PAGE is 30 kDa and its isoelectric point is 7.8. Immunofluorescence localization experiments with monoclonal antibodies specific for GP30-ASML and polyclonal antibodies raised against GP30-ASML showed this protein at the cell surface and in the lysosomal compartment of both cell lines; exclusively in the non metastatic variant it was also found in the nuclear membrane. The function of this protein is still unknown.
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PMID:Cell surface glycosylation and characterization of a differentially expressed glycoprotein in metastatic and non metastatic cell lines of the rat BSp73 tumor. 150 18

MPA induces mammary tumors in virgin BALB/c mice with an average latency of 52 weeks. In order to determine whether the simultaneous administration of a chemical carcinogen, N-methyl-N-nitrosourea (MNU), shortened the latency of MPA-induced tumors, a total of 60 virgin female BALB/c mice were treated with either MNU + MPA or MNU or MPA. The experiment lasted 7 months. The incidence and latency of mammary tumors were significantly different between the 3 groups: 15/19 (79%) in MNU + MPA-treated mice with a latency of 154 +/- 19 days; 3/20 (15%) in MNU-treated mice with a latency of 179 +/- 7 days; 0/20 (tumors only start appearing after 10 months) in MPA-treated mice. Histologically, MNU + MPA-induced tumors were similar to the few tumors observed in MNU-treated mice: most of them were type B adenocarcinomas with a high degree of necrosis and calcification. Only one of the MNU + MPA-induced tumors expressed high levels of ER and PR and proved to be MPA-responsive in further passages. All the other tumors showed low or non-detectable levels of ER and PR together with an independent pattern of tumor growth. In MNU-treated mice the only tumor that was transplanted proved to be hormone independent and had low levels of PR and ER. In both MNU and MNU + MPA treated mice lung adenocarcinomas were detected. Cystic uterine glandular hyperplasias were observed in all animals. It can be concluded that MPA and MNU potentiate their carcinogenic effect in mammary gland.
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PMID:Mammary carcinogenesis induced by N-methyl-N-nitrosourea (MNU) and medroxyprogesterone acetate (MPA) in BALB/c mice. 155 89

With the purpose of studying changes in the expression of glycoconjugate structures in nonmalignant and cancerous lesions of urothelium the lectins ConA, TKA, PNA, DBA, STA, LFA, UEA, MPA, RCA, LCA, GSA1, SBA, GSA2, WGA, PHA and Lot were tested in formalin-fixed, paraffin-embedded tissue sections of (1) cold biopsies from normal urothelium and bladder cancer of different grades (G1-G3) in humans, (2) normal transitional epithelium and N-butyl-N(4-hydroxybutyl)nitrosamine (BBN)-induced bladder cancer in animal experiments (Wistar rat), and (3) human transitional cancer cell line HT 1376. In human urothelium TKA and SBA were positive markers demonstrating positive staining reactions in all tumor grades without binding to normal epithelium. They stained also the human transitional carcinoma cell line HT 1376 (G3). In Wistar rats DBA, ConA, LCA, SBA, GSA2 and WGA had a specific affinity to BBN-induced carcinoma. Findings of positive lectin marker in transitional cell cancer may offer progress in diagnostics and therapy.
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PMID:Lectins in diagnosis of bladder carcinoma. 158 9

We present a case of a 25-year-old patient at term pregnancy who presented with a bilateral ovarian neoplasm that was histologically and immunohistochemically indistinguishable from ependymoma of the central nervous system. Progesterone receptors were detected in primary and recurrent neoplasms by immunohistochemistry. This is the first case of this rare neoplasm to present during pregnancy as well as with bilateral ovarian involvement. Together with a previously reported case of recurrent ovarian ependymoma with estrogen and progesterone receptors, this case suggests that hormonal responsiveness of this rare neoplasm may be pathogenically significant.
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PMID:Progesterone receptors in bilateral ovarian ependymoma presenting in pregnancy. 164 43


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